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Application of interferon response-related gene array to the antiviral treatment outcome in chronic hepatitis C

Tong-Jing Xing1, Hong-Tao Xv, Wei Zhao

  • 1Department Infectious Diseases, Taizhou People's Hospital, Taizhou 225300, China. xingtj518@sina.com.cn

Hepato-Gastroenterology
|March 18, 2011
PubMed
Abstract

Insights

Host genetic factors influence antiviral treatment response in chronic hepatitis C. Down-regulation of interferon response genes is linked to poor outcomes, particularly with hepatitis C virus genotype 1b.

Area of Science:

  • Hepatology
  • Immunology
  • Genetics

Background:

  • Viral factors like genotype and viral load impact antiviral treatment success.
  • Host genetic factors are increasingly recognized as crucial in modulating treatment responses.
  • Mechanisms behind variable virologic responses to interferon-alpha (IFNα) therapy remain unclear.

Purpose of the Study:

  • To investigate host gene expression differences in patients with chronic hepatitis C undergoing antiviral therapy.
  • To identify genetic factors associated with varying virologic response rates to IFNα-based treatment.

Main Methods:

  • RNA was isolated from peripheral blood monocytes of treatment-naïve chronic hepatitis C patients.
  • Gene expression profiling was performed using SuperArray microarrays.
  • Expression levels were compared between patients and healthy controls, and between different response groups.

Main Results:

  • Significant differences in gene expression were observed between rapid responders (RRs), non-RRs, and healthy controls.
  • Five differentially expressed genes were identified between RR and non-RR patient groups.
  • Hepatitis C virus (HCV) genotype 1b showed down-regulation of two genes compared to genotype 2a.
  • Seven genes were down-regulated in patients with end-of-treatment virologic response (ETVR) compared to non-ETVR.

Conclusions:

  • Down-regulation of interferon response-related genes correlates with a null response to interferon treatment.
  • HCV genotype 1b appears more effective at down-regulating interferon response genes than genotype 2a, contributing to treatment resistance.

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